Liver Disease Flashcards

1
Q

What are the important functions of the liver?

A

It is the major focus of synthetic, catabolic, and detoxifying activities in the body:

Metabolism of all food as well as some drugs (CYP450 enzymes)

Excretion of heme pigments

Important participant in immune response

Synthesis and storage of clotting factors (I, II, V, VII, IX, and X) vitK dependent factors are II, VII, IX, and X.

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2
Q

Why should dentists care about the liver function?

A

LA, analgesics, sedative, antibiotics, and antifungals are all metabolized in the liver.

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3
Q

What is hepatitis?

A

Liver inflammation

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4
Q

What causes hepatitis?

A

Infections or other causes:

Infectious causes = HAV, HBV, HCV, HDV, HEV, infectious mononucleosis, secondary syphillis, and tubercolosis.

Other causes = Excessive use of toxic substances inlcuding paracetamol, halothane, ketoconazole, methyldopa, methotrexate, and carbamezapine. Alcohol.

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5
Q

What causes most cases of hepatitis viral infections?

A

HAV, HBV, HCV. HAV is less common now due to more hygienic conditions.

HBV and HCV infections affect 540 million people worldwide. 370 million HBV and 170 million HCV. Causes considerable morbidity via cancer and cirrhosis.

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6
Q

How common is acute hepatitis?

A

Acute hepatitis affects approx 1% of people in the US with 80k new cases every year

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7
Q

How common is death from viral hepatitis?

A

Approximately 1 million deaths each year are caused by viral hepatitis

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8
Q

How are hepatitis A and E spread?

A

Most commonly via faecal oral route.

Occur in outbreaks as well as sporadically

Generally self limiting

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9
Q

What causes non-(A-E) hepatitis?

A

Unknown viral aetiology

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10
Q

How does hepatitis B, C, and D spread?

A

Parenteral routes most commonly and less commonly by intimate or sexual exposure.

Does not cause outbreak and can become chronic

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11
Q

How does viral hepatitis happen?

A

The virus is not directly cytopathic. Indirect damage occurs due to immune response by cytotoxic T-cell responses. Pro-inflammatory cytokines are involved as well as NK cells and antibody dependent cellular cytotoxicity.

Antibodies can provide partial immunity to reinfection

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12
Q

What is the clinical presentation of viral hepatitis?

A

Highly variable course: Transient, asymptomatic infection to severe or fulminant disease. Can be self-limited with complete resolution, relapsing, or chronic infection.

4 phases: Incubation, preicteric, icteric, and convalescence phase.

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13
Q

What is the incubation period in viral hepatitis?

A

Ranges from 2 to 20 weeks based on viral aetiologic agent and dose.

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14
Q

What are the potential complications of viral hepatitis?

A

Can be chronic or fulminant.

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15
Q

What happens during the incubation phase of viral hepatitis?

A

This is determined by the viral etiological agent and exposure dose.

The virus becomes detectable in the blood.

Antibody remains negative

The body has normal serum aminotransferase and bilirubin levels.

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16
Q

What happens during the preicteric phase?

A

Nonspecific symptoms: Fatigue, nausea, poor appetite, and vague upper right quadrant pain. Lasts 3 - 10 days.

During this phase virus specific antibodies are detectable.

Serum aminotransferase start to increase and viral load are highest in this phase

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17
Q

What happens durng the icteric phase?

A

Symptoms like jaundice, fatigue, and nausea worsen, hepato/splenomegaly in severe cases

Urine starts to darken in this stage.

Serum bilirubin levels are high

Aminotransferase enzymes are higher.

Viral load begins to lower.

Anorexia and weight loss common at this stage.

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18
Q

What happens during convalescence?

A

Can be prolonged

Neutralizing antibodies are highest at this stage.

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19
Q

What are the complications of acute viral hepititis?

A

Hepatic failure

1 - 2% of patients with symptomatic acute hepatitis. HBV > HCV

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20
Q

What are the complications of chronic hepatitis?

A

Illness of at least 6 months duration.

This develops in 2 - 7% of adults with hepB and 50 - 85% of adults with hepC

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21
Q

What are the signs of poor prognosis in hepatitis?

A

Persistently worsening jaundice, ascitis, decreased liver size, and higher thrombin time

22
Q

How is viral hepatitis diagnosed?

A

hepA: IgM anti-HAV

hepB: HBsAg, IgM anti-HBc

hepC: anti-HCV by EIA

hepD: HBsAg

hepE: History

Mononucleosis: History, WBC, differential counts

Drug-induced hepatitis: History

23
Q

How does alcoholic liver disease occur?

A

Alcohol is directly hepatotoxic and indirectly via acetyl aldehyde (which is fibrinogenic) and via cytokines.

24
Q

How do cytokines lead to alcohoic liver disease?

A

Alcohol induced influx of endotoxin (LPS) from gut into portal circulation leading to kuppfer cells -> Enhanced chemokine release -> damage to liver hepatocytes

25
Q

How much alcohol is enough to cause damage?

A

1 pint (~500ml) of whiskey for 10 years daily or several quarts of wine (1L)

26
Q

What deleterious effects does alcohol have on the body?

A

Neural development

Corticotropin releasing hormone system is negatively impacted by alcohol

Metabolism of neutrotransmitters

The function of neurotransmitter receptors

27
Q

What are the disease outcomes of long term alcohol consumption?

A

Impairment of the acetylcholine and dopaminergic systems leading to:

Sensory and motor disturbances (e.g., peripheral neuropathies)

Malnutrition (folic acid deficiency)

Anemias

Decreased immune function

Increased mortality rates

Hepatocellular carcinoma

Metastasis to liver

28
Q

What are the stages of alcoholic liver disease?

A

Fatty liver: Characterized by presence of fatty infiltrate, after only a moderate use of alcohol for a brief time. This is completely reversible

Alcoholic hepatitis: This is a diffuse inflammatory condition of the liver leading to destructive, irreversible cellular changes, this is reversible overall for the most part but can become irreversible.

Cirrhosis: This is irreversible, characterized by progressive fibrosis and abnormal regeneration of liver architecture resulting in progressive deterioration of liver function and then hepatic failure

29
Q

What are the features of hepatic failure?

A

Hepatic failure is characterized by oesophagitis, gastritis and pancreatitis leading to malnutrition, weight loss, protein deficiency, impaired coagulation, endocrine disturbances, jaundice, portal hypertension, oesophageal varices, increased ammonia production leading to encephalopathy, dementia, and psychosis,

This is in addition to cerebral degeneration upper gi tract cancer and liver cancer from heavy alcohol consumption.

30
Q

What is the clinical presentation of alcoholic liver disease?

A

Fatty liver: Possible enlargement.

Alcoholic hepatitis:

Nonspecific:

Nausea

Vomiting

Anorexia

Malaise

Weight loss

Fever

Specific:

Hepatomegaly

Splenomegaly

Jaundice

Ascites

Ankle oedema

Spider angiomas

31
Q

What are the symptoms early stage of alcoholic cirrhosis?

A

Can be asymptomatic until late stage.

Ascites

Spider angiomas

Ankle oedema

Jaundice

Haemorrhage from oesophageal varices

32
Q

What are the later signs of cirrhosis?

A

Hepatic encephalopathy

Coma

Death

33
Q

What are the nonspecific signs of cirrhosis?

A

Anaemia

Purpura

Ecchymosis

Gingival bleeding

Palmar erythema

Nail changes

Parotid gland enlargement

34
Q

What are the lab tests used for diagnosis of alcoholic liver disease?

A

Elevated bilirubin, alkaline phosphatase, AST, ALT, GGT, Amylase, Uric acid, and cholesterol.

Leukopenia or leucocytosis

Anaemia

Thrombocytopaenia

Carbohydrate deficient transferrin test

35
Q

What does the AST to ALT ratio tell us about alcoholic liver disease?

A

AST to ALT ratio above 2 is 90% predictive of alcoholic liver disease.

36
Q

What does GGT and corpuscular volume tell us about alcoholism?

A

GGT elevation and mean corpuscular volume are suggestive of alcoholism

37
Q

What does the carbohydrate deficient transferrin test tell us?

A

Monitor clniical status of alcohol dependency.

38
Q

What does thrombocytopaenia tell us about alcoholic liver disease?

A

Deficiencies of clotting factors can be told by prolonged PT and APTT

39
Q

How long will improvement take after ceasing alcohol consumption?

A

18 months there is improvement

40
Q

How should liver transplant patients be managed?

A

Pre-transplant dental care: dental clearance

Post transplant management: Multidisciplinary care, maintain oral hygiene and dental care, immunosuppression

41
Q

How long does liver damage take to progress to cirrhosis?

A

Median time is 30 years

Can take 5 - 50 years to develop

42
Q

How does liver damage accumulate?

A

Chronic injury leads to Inflammatory damage, matrix deposition, parenchymal cell death, angeiogenesis

This leads to disrupted archtecture, loss of function, and aberrant hepatocyte regeneration, eventually leading to cirrhosis

43
Q

How can accumulated damage of the liver be reversed?

A

Removal of the underlying cause and anti-fibrotic drug/cell therapy

44
Q

What are ALT, AST, GGT, and ALP used for?

A

They are markers of the disease and indicate the severity of hepatocellular damage

45
Q

What do albumin, bilirubin, and PT/INR indicate?

A

They are indicators of liver function

46
Q

How should patietns with alcoholic liver disease be managed?

A

Understand the possibilty of bleeding and infection. Consider

No need for abx prophylaxis. Avoid abx with liver metabolism

LA: Some are metabolised by the liver

Sedatives: Some are metabolised by the liver

Analgesics: Some are metabolised by the liver

47
Q

Which LAs are metabolised by the liver?

A

Lidocaine

Mepivacaine

Prilocaine

Bupivacaine

48
Q

Which analgesics are metabolised by the liver?

A

aspirin, paracetamol, codeine, ibuprofen, and meperidine

49
Q

Which sedatives are metabolised by the liver?

A

Diazepam

Barbiturates

50
Q

Which antibiotics are metabolized by the liver?

A

Ampicillin

Tetracycline

Metronidazole

Vancomycin

51
Q

What risks should be considered with alcoholic liver disease?

A

Safe dental care

Potential medical emergencies

Prescribing

Infection control

Impact on oral health

Consider referring